Circulating lipopolysaccharide-binding protein (LBP) as a marker of obesity-related insulin resistance
Objective: Lipopolysaccharide-binding protein (LBP) is a 65-kDa acute-phase protein present in blood at high concentrations, known to be derived from the liver. We aimed to gain insights into the association of circulating LBP with insulin resistance in humans and mice. Methods, design and measureme...
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Published in | International Journal of Obesity Vol. 36; no. 11; pp. 1442 - 1449 |
---|---|
Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
01.11.2012
Nature Publishing Group |
Subjects | |
Online Access | Get full text |
ISSN | 0307-0565 1476-5497 1476-5497 |
DOI | 10.1038/ijo.2011.256 |
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Abstract | Objective:
Lipopolysaccharide-binding protein (LBP) is a 65-kDa acute-phase protein present in blood at high concentrations, known to be derived from the liver. We aimed to gain insights into the association of circulating LBP with insulin resistance in humans and mice.
Methods, design and measurements:
We studied the cross-sectional (
n
=222) and weight loss-induced (
n
=34) associations of LBP (enzyme-linked immunosorbent assay) with inflammatory and metabolic parameters (including minimal model-measured insulin sensitivity), and the effects of high-fat diet (HFD), metformin and genetic insulin sensitization (glucagon-like peptide 1 receptor knockout model) in mice.
Results:
Circulating LBP concentration was significantly increased in subjects with type 2 diabetes and dramatically increased in subjects with morbid obesity. LBP was significantly associated with insulin sensitivity and different inflammatory markers and decreased after weight loss (22.2±5.8 vs 16.2±9.3 μg ml
−1
,
P
<0.0001) in association with changes in body mass index and insulin sensitivity. Circulating LBP concentration was increased in HFD mice, whereas decreased in glucagon-like peptide 1 receptor knockout mice (significantly more insulin sensitive than wild-type mice) and after metformin administration.
Conclusion:
LBP is an inflammatory marker associated with obesity-related insulin resistance. |
---|---|
AbstractList | OBJECTIVE: Lipopolysaccharide-binding protein (LBP) is a 65-kDa acute-phase protein present in blood at high concentrations, known to be derived from the liver. We aimed to gain insights into the association of circulating LBP with insulin resistance in humans and mice. METHODS, DESIGN AND MEASUREMENTS: We studied the cross-sectional (n = 222) and weight loss-induced (n = 34) associations of LBP (enzyme-linked immunosorbent assay) with inflammatory and metabolic parameters (including minimal model-measured insulin sensitivity), and the effects of high-fat diet (HFD), metformin and genetic insulin sensitization (glucagon-like peptide 1 receptor knockout model) in mice. RESULTS: Circulating LBP concentration was significantly increased in subjects with type 2 diabetes and dramatically increased in subjects with morbid obesity. LBP was significantly associated with insulin sensitivity and different inflammatory markers and decreased after weight loss (22.2 ± 5.8 vs 16.2 ±9.3 µg[ml.sup.-1], P<0.0001) in association with changes in body mass index and insulin sensitivity. Circulating LBP concentration was increased in HFD mice, whereas decreased in glucagon-like peptide 1 receptor knockout mice (significantly more insulin sensitive than wild-type mice) and after metformin administration. CONCLUSION: LBP is an inflammatory marker associated with obesity-related insulin resistance. International Journal of Obesity (2012) 36, 1442-1449; doi:10.1038/ijo.2011.256; published online 20 December 2011 Keywords: LBP;LPS;insulin resistance Lipopolysaccharide-binding protein (LBP) is a 65-kDa acute-phase protein present in blood at high concentrations, known to be derived from the liver. We aimed to gain insights into the association of circulating LBP with insulin resistance in humans and mice. METHODS, DESIGN AND MEASUREMENTS: We studied the cross-sectional (n=222) and weight loss-induced (n=34) associations of LBP (enzyme-linked immunosorbent assay) with inflammatory and metabolic parameters (including minimal model-measured insulin sensitivity), and the effects of high-fat diet (HFD), metformin and genetic insulin sensitization (glucagon-like peptide 1 receptor knockout model) in mice. Circulating LBP concentration was significantly increased in subjects with type 2 diabetes and dramatically increased in subjects with morbid obesity. LBP was significantly associated with insulin sensitivity and different inflammatory markers and decreased after weight loss (22.2 ± 5.8 vs 16.2 ± 9.3 μg ml(-1), P<0.0001) in association with changes in body mass index and insulin sensitivity. Circulating LBP concentration was increased in HFD mice, whereas decreased in glucagon-like peptide 1 receptor knockout mice (significantly more insulin sensitive than wild-type mice) and after metformin administration. LBP is an inflammatory marker associated with obesity-related insulin resistance. Objective: Lipopolysaccharide-binding protein (LBP) is a 65-kDa acute-phase protein present in blood at high concentrations, known to be derived from the liver. We aimed to gain insights into the association of circulating LBP with insulin resistance in humans and mice. Methods, design and measurements: We studied the cross-sectional ( n =222) and weight loss-induced ( n =34) associations of LBP (enzyme-linked immunosorbent assay) with inflammatory and metabolic parameters (including minimal model-measured insulin sensitivity), and the effects of high-fat diet (HFD), metformin and genetic insulin sensitization (glucagon-like peptide 1 receptor knockout model) in mice. Results: Circulating LBP concentration was significantly increased in subjects with type 2 diabetes and dramatically increased in subjects with morbid obesity. LBP was significantly associated with insulin sensitivity and different inflammatory markers and decreased after weight loss (22.2±5.8 vs 16.2±9.3 μg ml −1 , P <0.0001) in association with changes in body mass index and insulin sensitivity. Circulating LBP concentration was increased in HFD mice, whereas decreased in glucagon-like peptide 1 receptor knockout mice (significantly more insulin sensitive than wild-type mice) and after metformin administration. Conclusion: LBP is an inflammatory marker associated with obesity-related insulin resistance. International Journal of Obesity (2012) 36, 1442-1449; doi:10.1038/ijo.2011.256; published online 20 December 2011 Lipopolysaccharide-binding protein (LBP) is a 65-kDa acute-phase protein present in blood at high concentrations, known to be derived from the liver. We aimed to gain insights into the association of circulating LBP with insulin resistance in humans and mice. METHODS, DESIGN AND MEASUREMENTS: We studied the cross-sectional (n=222) and weight loss-induced (n=34) associations of LBP (enzyme-linked immunosorbent assay) with inflammatory and metabolic parameters (including minimal model-measured insulin sensitivity), and the effects of high-fat diet (HFD), metformin and genetic insulin sensitization (glucagon-like peptide 1 receptor knockout model) in mice.OBJECTIVELipopolysaccharide-binding protein (LBP) is a 65-kDa acute-phase protein present in blood at high concentrations, known to be derived from the liver. We aimed to gain insights into the association of circulating LBP with insulin resistance in humans and mice. METHODS, DESIGN AND MEASUREMENTS: We studied the cross-sectional (n=222) and weight loss-induced (n=34) associations of LBP (enzyme-linked immunosorbent assay) with inflammatory and metabolic parameters (including minimal model-measured insulin sensitivity), and the effects of high-fat diet (HFD), metformin and genetic insulin sensitization (glucagon-like peptide 1 receptor knockout model) in mice.Circulating LBP concentration was significantly increased in subjects with type 2 diabetes and dramatically increased in subjects with morbid obesity. LBP was significantly associated with insulin sensitivity and different inflammatory markers and decreased after weight loss (22.2 ± 5.8 vs 16.2 ± 9.3 μg ml(-1), P<0.0001) in association with changes in body mass index and insulin sensitivity. Circulating LBP concentration was increased in HFD mice, whereas decreased in glucagon-like peptide 1 receptor knockout mice (significantly more insulin sensitive than wild-type mice) and after metformin administration.RESULTSCirculating LBP concentration was significantly increased in subjects with type 2 diabetes and dramatically increased in subjects with morbid obesity. LBP was significantly associated with insulin sensitivity and different inflammatory markers and decreased after weight loss (22.2 ± 5.8 vs 16.2 ± 9.3 μg ml(-1), P<0.0001) in association with changes in body mass index and insulin sensitivity. Circulating LBP concentration was increased in HFD mice, whereas decreased in glucagon-like peptide 1 receptor knockout mice (significantly more insulin sensitive than wild-type mice) and after metformin administration.LBP is an inflammatory marker associated with obesity-related insulin resistance.CONCLUSIONLBP is an inflammatory marker associated with obesity-related insulin resistance. Objective: Lipopolysaccharide-binding protein (LBP) is a 65-kDa acute-phase protein present in blood at high concentrations, known to be derived from the liver. We aimed to gain insights into the association of circulating LBP with insulin resistance in humans and mice.Methods, design and measurements:We studied the cross-sectional (n=222) and weight loss-induced (n=34) associations of LBP (enzyme-linked immunosorbent assay) with inflammatory and metabolic parameters (including minimal model-measured insulin sensitivity), and the effects of high-fat diet (HFD), metformin and genetic insulin sensitization (glucagon-like peptide 1 receptor knockout model) in mice. Results: Circulating LBP concentration was significantly increased in subjects with type 2 diabetes and dramatically increased in subjects with morbid obesity. LBP was significantly associated with insulin sensitivity and different inflammatory markers and decreased after weight loss (22.2 plus or minus 5.8 vs 16.2 plus or minus 9.3 mu g ml super(-1), P<0.0001) in association with changes in body mass index and insulin sensitivity. Circulating LBP concentration was increased in HFD mice, whereas decreased in glucagon-like peptide 1 receptor knockout mice (significantly more insulin sensitive than wild-type mice) and after metformin administration. Conclusion: LBP is an inflammatory marker associated with obesity-related insulin resistance. Lipopolysaccharide-binding protein (LBP) is a 65-kDa acute-phase protein present in blood at high concentrations, known to be derived from the liver. We aimed to gain insights into the association of circulating LBP with insulin resistance in humans and mice. METHODS, DESIGN AND MEASUREMENTS: We studied the cross-sectional (n=222) and weight loss-induced (n=34) associations of LBP (enzyme-linked immunosorbent assay) with inflammatory and metabolic parameters (including minimal model-measured insulin sensitivity), and the effects of high-fat diet (HFD), metformin and genetic insulin sensitization (glucagon-like peptide 1 receptor knockout model) in mice. Circulating LBP concentration was significantly increased in subjects with type 2 diabetes and dramatically increased in subjects with morbid obesity. LBP was significantly associated with insulin sensitivity and different inflammatory markers and decreased after weight loss (22.2 ± 5.8 vs 16.2 ± 9.3 μgml(-1), P<0.0001) in association with changes in body mass index and insulin sensitivity. Circulating LBP concentration was increased in HFD mice, whereas decreased in glucagon-like peptide 1 receptor knockout mice (significantly more insulin sensitive than wild-type mice) and after metformin administration. LBP is an inflammatory marker associated with obesity-related insulin resistance. |
Audience | Academic |
Author | Luche, E Pardo, G Burcelin, R Serino, M Frühbeck, G Fernández-Real, J M Moreno-Navarrete, J M Waget, A Ortega, F Salvador, J Ricart, W |
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BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26580758$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/22184060$$D View this record in MEDLINE/PubMed |
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ContentType | Journal Article |
Copyright | Macmillan Publishers Limited 2012 2014 INIST-CNRS COPYRIGHT 2012 Nature Publishing Group Copyright Nature Publishing Group Nov 2012 |
Copyright_xml | – notice: Macmillan Publishers Limited 2012 – notice: 2014 INIST-CNRS – notice: COPYRIGHT 2012 Nature Publishing Group – notice: Copyright Nature Publishing Group Nov 2012 |
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Keywords | insulin resistance LPS LBP Endocrinopathy Human Obesity Pancreatic hormone Nutrition Rodentia Nutrition disorder Biological marker Metabolic diseases Protein A Insulin Binding protein Target tissue resistance Vertebrata Mammalia Mouse Lipopolysaccharide Insulin resistance Nutritional status |
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The common soil hypothesis revisited publication-title: Arterioscler Thromb Vasc Biol doi: 10.1161/01.ATV.0000122852.22604.78 – volume: 57 start-page: 2577 year: 2008 ident: BFijo2011256_CR21 publication-title: Diabetes doi: 10.2337/db08-0121 – volume: 56 start-page: 1761 year: 2007 ident: BFijo2011256_CR20 publication-title: Diabetes doi: 10.2337/db06-1491 – volume: 138 start-page: 2386 year: 2008 ident: BFijo2011256_CR27 publication-title: J Nutr doi: 10.3945/jn.108.092346 – volume: 57 start-page: 1470 year: 2008 ident: BFijo2011256_CR22 publication-title: Diabetes doi: 10.2337/db07-1403 – volume: 92 start-page: 3719 year: 2007 ident: BFijo2011256_CR19 publication-title: J Clin Endocrinol Metab doi: 10.1210/jc.2007-0349 – volume: 50 start-page: 25 year: 2007 ident: BFijo2011256_CR15 publication-title: J Am Coll Cardiol doi: 10.1016/j.jacc.2007.02.070 – volume: 24 start-page: 278 year: 2003 ident: BFijo2011256_CR5 publication-title: Endocr Rev doi: 10.1210/er.2002-0010 – volume: 102 start-page: 42 year: 2000 ident: BFijo2011256_CR3 publication-title: Circulation doi: 10.1161/01.CIR.102.1.42 – volume: 47 start-page: 1757 year: 1998 ident: BFijo2011256_CR26 publication-title: Diabetes doi: 10.2337/diabetes.47.11.1757 – volume: 79 start-page: 790 year: 1987 ident: BFijo2011256_CR17 publication-title: J Clin Invest doi: 10.1172/JCI112886 – volume: 179 start-page: 269 year: 1994 ident: BFijo2011256_CR12 publication-title: J Exp Med doi: 10.1084/jem.179.1.269 – volume: 346 start-page: 739 year: 2006 ident: BFijo2011256_CR7 publication-title: Biochem Biophys Res Commun doi: 10.1016/j.bbrc.2006.05.170 – volume: 55 start-page: 216 year: 2006 ident: BFijo2011256_CR14 publication-title: Diabetes doi: 10.2337/diabetes.55.01.06.db05-1108 – volume: 29 start-page: 1058 year: 2006 ident: BFijo2011256_CR8 publication-title: Diabetes Care doi: 10.2337/dc05-2068 – volume: 59 start-page: 200 year: 2010 ident: BFijo2011256_CR18 publication-title: Diabetes doi: 10.2337/db09-0700 – volume: 112 start-page: 1796 year: 2003 ident: BFijo2011256_CR1 publication-title: J Clin Invest doi: 10.1172/JCI200319246 – volume: 24 start-page: 816 year: 2004 ident: BFijo2011256_CR9 publication-title: Arterioscler Thromb Vasc Biol doi: 10.1161/01.ATV.0000122852.22604.78 – volume: 269 start-page: 8477 year: 1994 ident: BFijo2011256_CR10 publication-title: J Biol Chem doi: 10.1016/S0021-9258(17)37218-6 – volume: 33 start-page: 1629 year: 2010 ident: BFijo2011256_CR28 publication-title: Diabetes Care doi: 10.2337/dc09-1392 – volume: 8 start-page: 946 year: 2006 ident: BFijo2011256_CR23 publication-title: Microbes Infect doi: 10.1016/j.micinf.2005.10.006 – volume: 180 start-page: 1025 year: 1994 ident: BFijo2011256_CR13 publication-title: J Exp Med doi: 10.1084/jem.180.3.1025 – volume: 33 start-page: 1925 year: 2010 ident: BFijo2011256_CR16 publication-title: Diabetes Care doi: 10.2337/dc10-0340 – volume: 41 start-page: 1241 year: 1998 ident: BFijo2011256_CR2 publication-title: Diabetologia doi: 10.1007/s001250051058 – volume: 107 start-page: 391 year: 2003 ident: BFijo2011256_CR4 publication-title: Circulation doi: 10.1161/01.CIR.0000055014.62083.05 – volume: 264 start-page: 10867 year: 1989 ident: BFijo2011256_CR11 publication-title: J Biol Chem doi: 10.1016/S0021-9258(18)81700-8 – volume: 110 start-page: 650 year: 2011 ident: BFijo2011256_CR25 publication-title: J Appl Microbiol doi: 10.1111/j.1365-2672.2010.04922.x – volume: 21 start-page: 174 year: 2006 ident: BFijo2011256_CR6 publication-title: Mol Cell doi: 10.1016/S1016-8478(23)12877-9 – volume: 98 start-page: 3800 year: 2001 ident: BFijo2011256_CR24 publication-title: Blood doi: 10.1182/blood.V98.13.3800 |
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Lipopolysaccharide-binding protein (LBP) is a 65-kDa acute-phase protein present in blood at high concentrations, known to be derived from the... Lipopolysaccharide-binding protein (LBP) is a 65-kDa acute-phase protein present in blood at high concentrations, known to be derived from the liver. We aimed... OBJECTIVE: Lipopolysaccharide-binding protein (LBP) is a 65-kDa acute-phase protein present in blood at high concentrations, known to be derived from the... International Journal of Obesity (2012) 36, 1442-1449; doi:10.1038/ijo.2011.256; published online 20 December 2011 Objective: Lipopolysaccharide-binding protein (LBP) is a 65-kDa acute-phase protein present in blood at high concentrations, known to be derived from the... |
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Title | Circulating lipopolysaccharide-binding protein (LBP) as a marker of obesity-related insulin resistance |
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